It was time to test the 14 genes she had selected as the best candidates to reprogram a cell.

Using viruses to deliver the genes, she inserted all 14 at once into human cells. On the morning of July 1, 2006, Yu arrived at the lab and examined the culture dishes. Her eyes focused on a few colonies, each resembling a crowded city viewed from space. They looked like embryonic stem cells.
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Cells must pass certain tests. They must multiply for weeks while remaining in their delicate, primitive state. When they are allowed to develop, they must turn into all the other cell types.

Bad things happen. Cells develop too soon. Cells die. There is no “aha!” moment, Thomson has said, only stress. He looked at the colonies and suppressed any excitement. He told Yu, essentially: OK, well get back to me in a couple of weeks.
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In the fall of 2006, Yu was preparing to whittle down her list of genes when she fell ill. The pain in her gut was awful. She struggled to eat. Her doctor thought it was a stomach flu. Instead, in late October, Yu’s appendix burst. She was laid up for a month. When she returned to the lab, the problem with the culture medium struck again.

Not until January 2007 was she able to begin narrowing the list of genes. She spent several months testing subsets of them, finally arriving at four. Two, Oct4 and Sox2, were “Yamanaka factors,” the name given to the genes the Japanese scientist had used to reprogram mouse cells. Two, Nanog and Lin28, were not.

Using a virus to deliver the four genes, she reprogrammed a line of fetal cells, then repeated the experiments with more mature cells. Although the process was inefficient, succeeding with only a small fraction of cells, it did work.

At first their behavior might seem odd; to gather together in the face of starvation surely ought to end in cannibalism or death. Not so, for they are capable of an extraordinary and rare transformation. The amoebas set aside their lives as individuals and join ranks to form a new multicellular entity. Not all the amoebas will survive this cooperative venture, however. Some will sacrifice themselves to help the rest find a new life elsewhere.

These astonishing creatures are Dictyostelium discoideum, and they are a member of the slime mold family. They are also known as social amoebas. Aside from the novelty value of an organism that alternates between unicellular and multicellular existence, D. discoideum is highly useful in several areas of research. Among other things, this organism offers a stellar opportunity to study cell communication, cell differentiation, and the evolution of altruism.

In response to the cAMP distress call, up to one hundred thousand of the amoebas assemble. They first form a tower, which eventually topples over into an oblong blob about two millimeters long. The identical amoebas within this pseudoplasmodium– or slug– begin to differentiate and take on specialized roles.

Tool use is rare in wild animals, but of widespread interest because of its relationship to animal cognition, social learning and culture. Despite such attention, quantifying the costs and benefits of tool use has been difficult, largely because if tool use occurs, all population members typically exhibit the behavior. In Shark Bay, Australia, only a subset of the bottlenose dolphin population uses marine sponges as tools, providing an opportunity to assess both proximate and ultimate costs and benefits and document patterns of transmission.

We compared sponge-carrying (sponger) females to non-sponge-carrying (non-sponger) females and show that spongers were more solitary, spent more time in deep water channel habitats, dived for longer durations, and devoted more time to foraging than non-spongers; and, even with these potential proximate costs, calving success of sponger females was not significantly different from non-spongers. We also show a clear female-bias in the ontogeny of sponging. With a solitary lifestyle, specialization, and high foraging demands, spongers used tools more than any non-human animal. We suggest that the ecological, social, and developmental mechanisms involved likely (1) help explain the high intrapopulation variation in female behaviour, (2) indicate tradeoffs (e.g., time allocation) between ecological and social factors and, (3) constrain the spread of this innovation to primarily vertical transmission.

An analysis of the germs unleashed from a single commuter’s sneeze showed that within minutes they are being passed on via escalator handrails or seats on trains and underground carriages. At the busiest stations, one sneeze not smothered by a tissue or handkerchief will provide enough germs to infect another 150 commuters.
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A single sneeze expels 100,000 droplets of germs into the air at 90mph. Individual droplets get transferred to handles, rails and other areas frequently held or touched. Up to 10 per cent of all commuters will come into contact with an area infected by that one sneeze, Dr Henderson calculated.
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Researchers asked 1,300 workers about their health and found 99 per cent of commuters suffered at least one cold last winter. In contrast, just 58 per cent of those who work from home and 88 per cent of those who walk to work regularly caught a cold last winter.

Vanishing Arctic sea ice brought on by climate change is causing the crucially important microscopic marine plants called phytoplankton to bloom explosively and die away as never before, a phenomenon that is likely to create havoc among migratory creatures that rely on the ocean for food, Stanford scientists have found.
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Phytoplankton throughout the world’s oceans is the crucial nutrient at the base of the food web on which all marine life depends; when it’s plentiful, life thrives and when it’s gone, marine life is impossible.
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“It’s a complex system,” Arrigo said in an interview, “but as the changes in ice cover throw the timing of phytoplankton abundance off, then the birds and animals whose brains have long been programmed to migrate north at specific times of the year will have missed the boat if there’s no nourishment for them when they get there.”

Every spring and summer, phytoplankton in the Arctic blooms richly in explosive pulses, nourished by nitrogen and phosphorous in the seawater, and when those chemicals are consumed, the blooms end, Arrigo said.

Humans have an innate defence system against deadly bacteria. However, how the step from gene to anti-bacterial effect occurs in the body is not yet known. To date, B. Pseudomallei, a bacterium suitable for bioweapons, had managed to elude medics. It can remain hidden in the human body for many years without being detected by the immune system. The bacteria can suddenly become activated and spread throughout the body, resulting in the patient dying from blood poisoning. AMC physician Joost Wiersinga and the Laboratory for Experimental Internal Medicine discovered which gene-protein combination renders the lethal bacteria B. pseudomallei harmless.

Wiersinga focussed on the so-called Toll-like receptors. These are the proteins that initiate the fight against pathogens. There are currently ten known Toll-like receptors which are located on the outside of immune cells, our body’s defence system. The toll-like receptors jointly function as a 10-figure alarm code. Upon coming into contact with the immune cell each bacterium enters its own Toll code. For known pathogens this sets off an alarm in the immune system and the defence mechanism is activated. Yet B. pseudomallei fools the system by entering the code of a harmless bacterium. As a result the body’s defence system remains on standby.

Yet some people are resistant: they become infected but not ill. Wiersinga found a genetic cause for this resistance. He discovered which toll receptor can fend off B. pseudomallei. He did this by rearing mice DNA in which the gene for Toll2 production was switched on and off. ‘The group where the gene for Toll2 was switched off, survived the bacterial infection’, says Wiersinga. ‘The other receptor that we investigated, Toll4, had no effect - even though for the past ten years medics had regarded this as the most important receptor.’ The ultimate aim of this study is to develop a vaccine.

Dieticians at Addenbrooke’s have said evidence suggested the yoghurt might cut the risk of contracting C.diff. Caroline Heyes, dietetic services manager at Addenbrooke’s hospital, said: “Probiotic yoghurts may play a role in preventing C.difficile infection so we have been running a pilot on three of the care of the elderly wards for six months.
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“We can’t say for sure how much of that benefit is down to the yoghurt and how much they are down to a whole range of infection control procedures that the hospital has in place such as the deep cleaning programme, the bare-below-the-elbow programme, and the increased isolation procedures,” Ms Heyes said.

“We’re all sterile until we’re born,” says Glenn Gibson, a microbiologist at the University of Reading in Britain. “We haven’t got anything in us right up until the time we come into this big, bad, dirty world.”

But as soon as we pass out of the birth canal, when we are fetched by a doctor’s hands, placed in a hospital crib, put on our mother’s breast, when we drag a thumb across a blanket and stick that thumb in our mouths, when we swallow our first soft food, we are invaded by all sorts of bacteria. Once inside, they multiply - until the bacteria inside us outnumber our human cells.
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University of Chicago immunologist Alexander Chervonsky, with collaborators from Yale University, recently reported that doses of the right stomach bacteria can stop the development of type 1 diabetes in lab mice. “By changing who is living in our guts, we can prevent type 1 diabetes,” he told The Wall Street Journal.

The bottom line: We now have two sets of genes to think about - the ones we got from our parents and the ones of organisms living inside us. Our parents’ genes we can’t change, but the other set? Now that is one of the newest and most exciting fields in cell biology.

You could have two people sitting down to a bowl of cheerios, they could each eat the same number of cheerios but because of a difference in their gut bacteria one will get more calories than the other.

Entomologist Jennifer Zaspel at the University of Florida in Gainesville said the discovery suggests the moth population could be on an “evolutionary trajectory” away from other C. thalictri populations.

In January, she will compare the Russian population’s DNA to that of other populations and other species to confirm her suspicions. “Based on geography, based on behavior, and based on a phenotypic variation we saw in the wing pattern, we can speculate that this represents something different, something new,” Zaspel said.
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Only male moths exhibit blood feeding, she noted, raising the possibility that as in some species of butterflies and other moths, the Russian moths do it to pass on salt to females during copulation.

“There is no evidence it prolongs the life of the male, or anything like that,” she said. “So we suspect that it is probably going to the female.” The sexual gift, she said, would provide a nutritional boost to young larvae that feed on leaf-rich, but sodium-poor, diets.

A common mistake amongst non apiarists is the assumed fact that the queen directly controls the hive. Effectively, however, her duty is as an egg making machine. She can lay bout two thousand eggs a day in the spring. This amounts to more than her own weight in eggs each day. Surrounded continuously by workers, she needs for nothing. They give her food and take her waste away. They will also collect a pheromone which they then distribute to stop workers from starting queen cells.
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This very close up [follow link] of a queen bee shows one of its greatest - and smallest - enemies. The bee mite is an external parasite that attacks honey bees. It attaches itself to the bee’s body and sucks out its hemolymph. This is the blood analogue that is used by bees as they have an open circulatory system. Unfortunately the mite is more than just a pain in the neck. It can spread a host of viruses, including “Deformed Wing Virus” and the arrival of mites in a colony can often spell its demise. Scientists believe that the mite may contribute to the Colony Collapse Disorder (otherwise known as CCD) that is spreading throughout the United States.

It also makes perfect sense that our bodies evolved to store energy for worse times (and some of us have bodies better at doing that). Now we are in a new environment where (at least for many people alive today) finding enough calories is not going to be a problem so it would be nice if we could tell our bodies to get less efficient at storing fat

“Today the Broad Institute is the world’s leading genomics and biomedical institute, and we’re now making a $600 million bet that the Broad will be the place where the greatest scientific discoveries take place,” Eli Broad said at today’s ceremony.
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In its short history, the Broad Institute’s accomplishments include cataloging and identifying genetic risk factors for diseases such as type 2 diabetes and autism; discovering new therapeutic targets for cancer, malaria, and other diseases; and applying genomic tools to better understand and treat human pathogens like tuberculosis.
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The Broads’ gift is the largest to support biomedical research at a university anywhere in the world. The Broads initially invested $100 million in 2003 as a way to test the institute’s new approach to biomedical research. By 2005, the Broad Institute had already made significant accomplishments and progress, and the Broads invested a second $100 million. Their endowment of $400 million today will allow the Broad Institute to transition to a permanent, non-profit 501(c)(3) organization with both Harvard and MIT still at the heart of it, continuing to help govern the institute.

An ant so unlike all other living ants that it was given an extraterrestrial name has been discovered in the Amazon rain forest, biologists announced today. The tiny new species is the only known surviving member of an ant lineage that separated from the main family more than a hundred million years ago, DNA analysis revealed.

The pale, eyeless ant appears to be adapted to living underground, possibly surfacing at night to forage. Its long mandibles suggest that the 0.08-inch-long (2-millimeter-long) animal is a predator, most likely of soft-bodied creatures such as termite larvae.

Christian Rabeling, a graduate student at the University of Texas in Austin, found a single specimen of the new species, thought to be a worker ant, in tropical soils near Manaus, Brazil. Rabeling’s team named the new creature Martialis heureka—”Martialis” means “of Mars
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The new species’ genes suggest that it broke away from the main ant family before the origin of all other living ant groups, which include 20 subfamilies that together contain more than 12,000 species.

Autism isn’t like tuberculosis, there’s not a bacteria that causes the disease. In fact,most researchers believe that “autism” is not a discrete disorder, rather “autism is a clinically defined pervasive developmental disorder with phenotypically diverse neuropsychiatric symptoms and characteristics. These manifest as a spectrum of social and communicative deficits, stereotypical patterns and disturbances of behaviour.”¹
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If a particular trait’s heritability is 100% then the trait is due entirely to genetic variation, if the heritability is 0% then the trait is due entirely to environmental variation. By some estimates, heritability of autism spectrum disorders exceeds 90%
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repeated studies have found that autism diagnoses continue to rise even after the removal of thimerosal from the vaccine.
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Finally, when thinking about the environmental influences on autism, it’s important to explore the role of the environment on genetics. Many of the types of genetic changes that have been identified as causative in autism are indicative of some sort of DNA damage - DNA damage that may result from exposure to an environmental toxin. Many scientists, and I count myself in their number, feel that the recent autism ‘epidemic’ is due primarily to improved screening and diagnosis. In other words, prior to the 1980’s, many people suffering from autism were diagnosed as “slow” or misdiagnosed with another type of mental retardation. Unfortunately, there is no way to quantify this hypothesis.

Ever since, a 30 km ‘exclusion zone’ has existed around the contaminated site, accessible to those with special clearance only. It’s quite easy, then, to conjure an apocalyptic vision of the area; to imagine an eerily deserted wasteland, utterly devoid of life.

But the truth is quite the opposite. The exclusion zone is teeming with wildlife of all shapes and sizes, flourishing unhindered by human interference and seemingly unfazed by the ever-present radiation. Most remarkable, however, is not the life buzzing around the site, but what’s blooming inside the perilous depths of the reactor.

Sitting at the centre of the exclusion zone, the damaged reactor unit is encased in a steel and cement sarcophagus. It’s a deathly tomb that plays host to about 200 tonnes of melted radioactive fuel, and is swarming with radioactive dust.

But it’s also the abode of some very hardy fungi which researchers believe aren’t just tolerating the severe radiation, but actually harnessing its energy to thrive.

“Our findings suggest that [the fungi] can capture the energy from radiation and transform it into other forms of energy that can be used for growth,” said microbiologist Arturo Casadevall from the Albert Einstein College of Medicine at Yeshiva University in New York, USA.
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Taken together, the researchers think their results do indeed hint that fungi can live off ionising radiation, harnessing its energy through melanin to somehow generate a new form of biologically usable growing power.

If they’re right, then this is powerful stuff, said fungal biologist Dee Carter from the University of Sydney. The results will challenge fundamental assumptions we have about the very nature of fungi, she said.

It also raises the possibility that fungi might be using melanin to secretly harvest visible and ultraviolet light for growth, adds Casadevall. If confirmed, this will further complicate our understanding of these sneaky organisms and their role in ecosystems.